Bacterial infection in the pathogenesis of variceal bleeding

Variceal bleeding is a life-threatening complication of cirrhosis. Potential risk factors include clinical, endoscopic, and haemodynamic factors, but why bleeding occurs unpredictably in individual patients is not known. We postulate that bacterial infections in patients with variceal haemorrhage ma...

Full description

Saved in:
Bibliographic Details
Published in:The Lancet (British edition) 1999-01, Vol.353 (9147), p.139-142
Main Authors: Goulis, John, Patch, David, Burroughs, Andrew K
Format: Article
Language:English
Subjects:
Bacterial diseases
Bacterial Infections - microbiology
Bacterial Infections - physiopathology
Biological and medical sciences
Endothelins - physiology
Endotoxins
Endotoxins - blood
Esophageal and Gastric Varices - microbiology
Esophageal and Gastric Varices - physiopathology
Esophagus
Gastroenterology. Liver. Pancreas. Abdomen
Gastrointestinal Hemorrhage - microbiology
Gastrointestinal Hemorrhage - physiopathology
Hemorrhage
Hemostasis - physiology
Humans
Infections
Liver - blood supply
Liver cirrhosis
Medical diagnosis
Medical sciences
Nitric oxide
Nitric Oxide - physiology
Other diseases. Semiology
Portal Pressure - physiology
Risk Factors
Vascular Resistance - physiology
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Variceal bleeding is a life-threatening complication of cirrhosis. Potential risk factors include clinical, endoscopic, and haemodynamic factors, but why bleeding occurs unpredictably in individual patients is not known. We postulate that bacterial infections in patients with variceal haemorrhage may be the critical factor that triggers bleeding. In patients with large varices and a high wall tension, the release of endotoxin into the systemic circulation during episodes of bacterial infection results in a further increase in portal pressure through the induction of endothelin and possibly vasoconstrictive cyclo-oxygenase products. The subsequent contraction of hepatic stellate cells causes a rise in intrahepatic vascular resistance. Furthermore, endotoxin-induced nitric oxide and prostacyclin, and prostacyclin induced by endothelin could inhibit platelet aggregation, which may result in a further deterioration of primary haemostasis at the level of varix. We propose that the combination of these two effects leads to the onset of variceal haemorrhage.
ISSN:0140-6736
1474-547X
DOI:10.1016/S0140-6736(98)06020-6